ライフサイエンスコーパス: ANP

1 ANP (atrial natriuretic peptide) and BNP (B-type natriur

2 ANP acting through natriuretic peptide receptor-A (NPRA)

3 ANP and cGMP inhibited TGF-beta1-induced myofibroblast t

4 ANP and mANP also had opposing effects on ICa,L in human

5 ANP augmented insulin secretion at the threshold glucose

6 ANP blocks vascular endothelial growth factor (VEGF) pro

7 ANP effects were mediated by the Rac1 GTPase effector PA

8 ANP greatly enhances the phosphorylation at Ser-239 of t

9 ANP increased AP upstroke velocity (Vmax), AP duration,

10 ANP increased haematocrit from 40.6% to 46.8%, correspon

11 ANP is a member of the natriuretic peptide (NP) family,

12 ANP is an important biomarker of heart failure where low

13 ANP rapidly and substantially increased with initiation

14 ANP reduced the response of ARPE-19 cells to VEGF apical

15 ANP significantly reversed VEGF-induced BRB TEER reducti

16 ANP's TEER response was concentration but not time depen

17 ANP(1-28) remained unchanged, while NT-ANP(1-98) was red

18 ovirus showed increased expression of Cav-3, ANP, and Akt phosphorylation.

19 e with lower baseline concentrations (+44%); ANP increases were sustained.

20 or purified neutral endopeptidase to abolish ANP-dependent activation of NPR-A.

21 Finally, adding ANP to the Corin-deficient HK-2 conditioned medium rescu

22 Additionally, ANP and BNP were found to be the natural ligands for cel

23 ets, before and after saline administration, ANP levels were up to 50% higher in AG individuals than

24 le and skin microvascular permeability after ANP.

25 Although ANP and BNP are well-characterized regulators of blood p

26 An ANP gradient was developed, allowing for the direct anal

27 NP (1 pM to 1 micromol/L), and/or isatin, an ANP receptor antagonist.

28 Because both ASK1 and ANP are associated with pathologic cardiac hypertrophy,

29 d higher in 293 compared with HeLa cells and ANP did not increase internalization of FLAG-GC-A.

30 These results indicate that corin and ANP are essential for physiological changes at the mater

31 Corin and ANP expression in DN rat kidneys and high-glucose-treate

32 e found a significant reduction in Corin and ANP expression in DN rat kidneys.

33 erface, suggesting that defects in corin and ANP function may contribute to pre-eclampsia.

34 Here we identify a new function of corin and ANP in promoting trophoblast invasion and spiral artery

35 nocyte progenitors that express both MDR and ANP.

36 , but a gene dosage-dependent drop in atrial ANP and BNP content occurred.

37 n in cultured mesangial cells and attenuated ANP-mediated relaxation of aortic rings ex vivo.

38 that the PDE4 inhibitor rolipram attenuates ANP-induced increases in vascular permeability after inf

39 ANPs containing trisubstituted nitrogen (aza-ANPs) has been synthesized.

40 The aza-acyclic nucleoside phosphonates (aza-ANPs) are good inhibitors of Plasmodium falciparum HGXPR

41 t that the different affinities of these aza-ANPs could be due to the flexibility of the loops surrou

42 Prodrugs of these aza-ANPs exhibit antimalarial activity against Pf lines with

43 y a candidate route of communication between ANP and its receptors on the external membrane of smooth

44 p.Ile138Thr inhibits the interaction between ANP and its receptor natriuretic peptide receptor A and

45 f these were located on the mature bioactive ANP itself.

46 e-specific O-glycosylation shields bioactive ANP from proteolytic degradation and modifies potency at

47 FLAG-GC-A bound ANP identically with wild-type GC-A and was internalized

48 n of particulate guanylate cyclase (GC-A) by ANP leads to a substantial, dose-dependent, rapid, and s

49 hances the stimulation of NPR-A and NPR-B by ANP and CNP, respectively.

50 ioma cells through either stimulating pGC by ANP/BNP, or blocking PDE by 3-isobutyl-1-methylxanthine/

51 mechanism of vascular barrier protection by ANP via modulation of GEF-H1 function.

52 se in net apical-to-basal fluid transport by ANP (5 muM) that was inhibited completely by the ANP rec

53 ite: increased with SIL+ISO but unaltered by ANP+ISO.

54 on attenuates acute renal and cardiovascular ANP actions in vivo The discovery of novel glycosylated

55 ing enzyme (IDE) was found to rapidly cleave ANP, but the functional consequences of such cleavages i

56 IDE rapidly cleaves ANP and CNP, thus inactivating their ability to raise in

57 aneously demonstrated a lack of compensatory ANP elevation in advanced hypertension.

58 At low concentrations, ANP and beta-AR agonists additively enhanced expression

59 lation of secretory granules (SG) containing ANP propeptides (pro-ANP), a signature of maladaptive hy

60 In contrast, ANP elicited sustained submembrane elevations in [cGMP](

61 ors of PDE3A mimicked the effect of low-dose ANP on thrombin-induced permeability, and inhibition of

62 In pulmonary ECs, ANP suppressed thrombin-induced disassembly of periphera

63 Studies on the gene encoding ANP (NPPA) initiated the field of modern research into g

64 nding to the mRNA of NPPA, the gene encoding ANP.

65 locus containing the adjacent genes encoding ANP and BNP harbored 4 independent cis variants with eff

66 e with selective deletion of the endothelial ANP receptor.

67 lar permeability after infusion of exogenous ANP and observations of elevated central venous pressure

68 detected in mice grafted with HSE expressing ANP from either keratinocytes or fibroblasts, and topica

69 These data indicate that the familial ANP mutation associated with atrial fibrillation has onl

70 It is the first ANP derivative with such potent antimalarial activity an

71 pressing wild-type NPR-A (P<=4.13x10(-5) for ANP and P<=4.24x10(-3) for BNP).

72 ompanied by increased protein expression for ANP and BNP.

73 etion of the guanylyl cyclase-A receptor for ANP.

74 ost 30% of whole body clearance required for ANP to regulate plasma volume.

75 human and animal studies indicate a role for ANP as a regulator of blood pressure with conflicting re

76 Further, ANP and BNP elicit increases in blood microvessel permea

77 e.g., TNFalpha), hypertrophic factors (e.g., ANP), and profibrotic factors (e.g., TGFbeta1) from both

78 At 6 mmol/L glucose, ANP readily elicited Ca(2+) influx in control beta-cells

79 in vivo The discovery of novel glycosylated ANP proteoforms reported here significantly improves our

80 at failed to associate with pro-ANP hindered ANP-mediated protection against hypertrophy, which was r

81 rmore, mice with HSE grafts expressing human ANP did not develop elevated blood pressure when fed a h

82 Mice with elevated plasma levels of human ANP showed lower renin levels and, correspondingly, had

83 Significant plasma levels of human ANP were detected in mice grafted with HSE expressing AN

84 scan for sequence variants within the human ANP gene, a mutation was identified that results in a 40

85 In 293 cells, (125)I-ANP and (125)I-IgG uptake curves were superimposable bec

86 HeLa cells endogenously express GC-A, (125)I-ANP binding and cross-linking studies only detected NPR-

87 n part, because previous studies used (125)I-ANP binding to track these receptors, which are expresse

88 n following 10 min of treatment with Ang II, ANP or 8-bromo-cGMP.

89 n mice results in dysmorphic LDCVs, impaired ANP secretion, and hypertension.

90 In ANP mixotrophic fermentation, the two molecules of CO2 a

91 Change in ANP, MR-proANP, BNP (using 5 assays), NT-proBNP (3 assay

92 ein levels dropped, followed by a decline in ANP precursor (proANP) levels.

93 (TRAP/HTV), which was further exacerbated in ANP(-/-) mice.

94 n, a PI3K inhibitor, blocked the increase in ANP expression.

95 e, relative to the corresponding increase in ANP-induced renal water excretion.

96 challenge is associated with a reduction in ANP production.

97 ull-length PS1 (inactive gamma-secretase) in ANP.24 cells.

98 ition may be partially mediated by increased ANP concentrations.

99 lacking functional KATP channels (SUR1-KO), ANP increased electrical activity, suggesting no involve

100 or lumpectomy with an axillary procedure (L-ANP).

101 tomy carries higher complication rate than l-ANP with wound infection being the most common.

102 PDE2 mediates ANP/cGMP-induced decreases in aldosterone production.

103 In mice, ANP and mANP (10-100 nmol/L) had opposing effects on atr

104 helial (ARPE-19) cells with VEGF (10 ng/ml), ANP (1 pM to 1 micromol/L), and/or isatin, an ANP recept

105 Either modified ANP plasma levels or peptide structural alterations have

106 miR-155 and miR-105, were found to modulate ANP production in human cardiomyocytes and target geneti

107 Moreover, ANP potentiated the effect of glucagon-like peptide 1 (G

108 Increased expression of phospho-mTOR, ANP, and SERCA2a also suggests that T(3) promotes matura

109 We have termed this peptide mutant ANP.

110 ng and follow-up analyses showed that mutant ANP (mANP) activates multiple innate immunity pathways,

111 ic or diuretic response with low-dose native ANP.

112 ults in a 40-AA peptide consisting of native ANP((1-28)) and a C-terminal extension of 12 AA.

113 nal blood flow enhancing actions than native ANP in vivo.

114 owering properties when compared with native ANP.

115 allenge causes an upregulation of a negative ANP regulator microRNA-425 (miR-425), which reduces ANP

116 For FLAG-NPR-C, neither ANP, BNP, nor CNP increased its internalization in eithe

117 In contrast, neither ANP nor mANP had any effect on Na(+) current in mouse at

118 th human HGPRT have led to the design of new ANPs.

119 Akt phosphorylation was inhibited by 100 nm ANP.

120 ncreased by 4-fold in the presence of 100 nm ANP.

121 Notably, ANP abolished spontaneous contraction amplitude (P = 0.0

122 Notably, ANPs are also required for both the elicitor-induced oxi

123 rmined, three of these in complex with novel ANPs and one with GMP and pyrophosphate.

124 end toward lower levels of plasma atrial NP (ANP) and significantly smaller levels of cyclic guanosin

125 In human adipocytes, atrial NP (ANP) and ventricular NP (BNP) activated PPARgamma coacti

126 Three distinct NPs (ANP, BNP, and CNP) can selectively activate natriuretic

127 ANP(1-28) remained unchanged, while NT-ANP(1-98) was reduced in pre-hypertension (p < 0.05).

128 of IDE expression diminishes the ability of ANP and BNP to stimulate NPR-B.

129 The action of ANP and rolipram to modify albumin clearances in duodenu

130 l contribution to the hypovolaemic action of ANP can be measured by the magnitude of the ANP-induced

131 l molecular mechanism by which activation of ANP/cGMP/protein kinase G signaling disrupts TGF-beta1-i

132 The activity of ANP may in part be cGMP dependent, as 8-bromo-cGMP had s

133 t they affect both stability and activity of ANP.

134 3',5'-guanosine monophosphate) on binding of ANP, BNP (atrial or brain natriuretic peptide).

135 activity-related musclin-dependent boost of ANP/cGMP signaling results in significantly lower maximu

136 In this review, we define the bounds of ANP mixotrophy, calculate the potential metabolic advant

137 Additionally, the cleavages of ANP and BNP by IDE render them active with NPR-B and a r

138 s affecting the circulating concentration of ANP associated with blood pressure, whereas those affect

139 le further evaluation of the contribution of ANP-dependent microvascular beds (such as gastro-intesti

140 entricular myocytes (RV), the lowest dose of ANP (0.003 nm) inhibited Ang II-stimulated BrdU uptake b

141 on of permeability seen with higher doses of ANP.

142 ition of permeability caused by low doses of ANP.

143 ghting the blood pressure-lowering effect of ANP in the general population.

144 The protective effects of ANP against TRAP/HTV-induced lung injury were linked to

145 These effects of ANP and BNP on contractile function were examined furthe

146 etic and endothelial permeability effects of ANP cooperate in intravascular volume regulation.

147 The current study evaluated effects of ANP on beta-cell function by the use of a beta-cell-spec

148 ated by cAMP Epac pathways in the effects of ANP on beta-cell function; the latter seems to prevail.

149 more sensitive to the inhibitory effects of ANP than the LV (P < 0.0001).

150 cross-sectional area, and the expression of ANP (atrial natriuretic peptide) were significantly atte

151 esults in the generation of a mutant form of ANP (mANP), was identified and shown to cause atrial fib

152 and assessment of different plasma forms of ANP and BNP.

153 rats treated with intravitreal injections of ANP, VEGF, or vehicle.

154 lar wall thickness, increased lung levels of ANP (atrial natriuretic peptide), BNP (brain-type natriu

155 ed HSE resulted in persistent high levels of ANP expression in vivo.

156 Atrial and serum levels of ANP fell sharply in PAM myosin heavy chain 6 conditional

157 Magnitude of ANP increase was greatest in those with concentrations a

158 demonstrates a novel protective mechanism of ANP against pathologic hyperpermeability and suggests a

159 rt, we have discovered that the precursor of ANP, natriuretic peptide precursor (NPPA), physically in

160 s study identifies miR-425 as a regulator of ANP production, raising the possibility that miR-425 ant

161 acid 425 (miR-425), a negative regulator of ANP, were examined.

162 tools to identify novel miRNA regulators of ANP production that could be targeted to raise ANP level

163 nse of NPR-A and NPR-B to the stimulation of ANP, BNP, and CNP in cultured cells.

164 stone deacetylase 4 (HDAC4), upregulation of ANP and BNP in failing hearts did not require increased

165 Here, a novel class of ANPs containing trisubstituted nitrogen (aza-ANPs) has b

166 id foundation for the further development of ANPs as selective inhibitors of MtHGPRT and as antituber

167 tabilizing the endothelial barrier to offset ANP-induced increases in vascular permeability may be pa

168 nhanced the repressive effects of miR-425 on ANP production in human cardiomyocytes.

169 y of alcohol dependence via its influence on ANP and amygdala processing.

170 We show that pregnant corin- or ANP-deficient mice developed high blood pressure and pro

171 The effect of Corin-siRNA or ANP-siRNA HK-2 cells on EA.hy926 cell migration was dete

172 with conditioned medium from Corin-siRNA- or ANP-siRNA-transfected HK-2 cells was determined by weste

173 nopyrimidine (PMEO-DAPym) differs from other ANPs in that the aliphatic alkyloxy linker is bound to t

174 Aggregated nanogel particles (ANPs) were generated by aggregating GNPs to micron-size,

175 tective peptides atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in heart tissu

176 myocytes secrete atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in response to

177 peptides (NPs), atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP), have central

178 uretic peptides, atrial natriuretic peptide (ANP) and B-type or brain natriuretic peptide (BNP), in t

179 nucleic acid for atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were increased

180 ogram, including atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), is a hallmark

181 uretic factor or atrial natriuretic peptide (ANP) and brain or B-type natriuretic peptide (BNP), ther

182 hway in RPE with atrial natriuretic peptide (ANP) and with membrane-permeable analogs of cGMP would i

183 Atrial natriuretic peptide (ANP) binds guanylyl cyclase-A (GC-A) and natriuretic pep

184 Atrial natriuretic peptide (ANP) binds guanylyl cyclase-A/natriuretic peptide recept

185 PA) encoding the atrial natriuretic peptide (ANP) causes inflammation, fibroblast activation, atrial

186 ril/valsartan on atrial natriuretic peptide (ANP) concentrations in patients are unknown.

187 acts as the pro-atrial natriuretic peptide (ANP) convertase.

188 impact of rs5065 atrial natriuretic peptide (ANP) gene variant on coronary artery disease (CAD) and i

189 c variant of the atrial natriuretic peptide (ANP) gene.

190 as 10 micromol/L atrial natriuretic peptide (ANP) had no effect.

191 Atrial natriuretic peptide (ANP) has a central role in regulating blood pressure in

192 The role of atrial natriuretic peptide (ANP) in regulating fetal cardiac growth is poorly unders

193 c oxide (NO) and atrial natriuretic peptide (ANP) induced synthesis of intracellular cGMP, [cGMP](i).

194 Atrial natriuretic peptide (ANP) influences glucose homeostasis and possibly acts as

195 cardiac hormone atrial natriuretic peptide (ANP) is a 28-amino acid (AA) peptide that consists of a

196 Atrial natriuretic peptide (ANP) is a hormone with diuretic, natriuretic, and vasodi

197 Atrial natriuretic peptide (ANP) is a hormone with numerous beneficial cardiovascula

198 Atrial natriuretic peptide (ANP) is a peptide hormone that in response to atrial str

199 Atrial natriuretic peptide (ANP) is an endogenous peptide hormone that is synthesize

200 Although atrial natriuretic peptide (ANP) is not amidated, Pam expression in the atrium excee

201 on of endogenous atrial natriuretic peptide (ANP) to increase vascular permeability to the plasma pro

202 Atrial natriuretic peptide (ANP) via its guanylyl cyclase-A (GC-A) receptor particip

203 ulating chimeric atrial natriuretic peptide (ANP) was detected in high concentration in subjects with

204 he C terminus of atrial natriuretic peptide (ANP) was recently genetically linked to patients with fa

205 e that activates atrial natriuretic peptide (ANP), a cardiac hormone that is important in regulating

206 on by expressing atrial natriuretic peptide (ANP), a hormone able to decrease blood pressure, in bioe

207 ces secretion of atrial natriuretic peptide (ANP), a regulator of blood pressure and natriuresis.

208 ng region of the A-type natriuretic peptide (ANP), demonstrating that they affect both stability and

209 he gene encoding atrial natriuretic peptide (ANP), is associated with blood pressure.

210 The receptor for atrial natriuretic peptide (ANP), natriuretic peptide receptor A (NPRA), is expresse

211 y in response to atrial natriuretic peptide (ANP), which acts with the kidney to regulate plasma volu

212 protein in both atrial natriuretic peptide (ANP)-dependent and -independent manner.

213 ial regulator of atrial natriuretic peptide (ANP)-mediated counterhypertrophic responses in cardiomyo

214 y treatment with atrial natriuretic peptide (ANP).

215 iption factor of atrial natriuretic peptide (ANP).

216 at activation of atrial natriuretic peptide (ANP)/cGMP/protein kinase G signaling inhibits transformi

217 either atrial nor brain natriuretic peptide (ANP, BNP) is amidated, the major membrane protein in atr

218 onstrictive) and atrial natriuretic peptide (ANP; vasodilatory) antagonize the biological actions of

219 served that the cardiac natriuretic peptides ANP and BNP and the guanylate cyclase-linked natriuretic

220 e species, the cardiac natriuretic peptides (ANP and BNP) are produced by cardiomyocytes in the devel

221 Atrial and brain natriuretic peptides (ANP and BNP, respectively) are cardiac hormones released

222 d and quantified under aqueous normal phase (ANP) conditions, using a Diamond Hydride (DH) column for

223 : reversed phase (RP), aqueous normal phase (ANP), and hydrophilic interaction (HILIC) for the analys

224 beta-modified acyclonucleoside phosphonate (ANP) derivatives, using commercially available and inexp

225 e acyclic pyrimidine nucleoside phosphonate (ANP) phosphonylmethoxyethoxydiaminopyrimidine (PMEO-DAPy

226 Acyclic nucleoside phosphonates (ANPs) are inhibitors of HG(X)PRT and arrest the growth o

227 synthesized acyclic nucleoside phosphonates (ANPs) have been shown to be competitive inhibitors of Mt

228 Acyclic nucleoside phosphonates (ANPs) that contain a 6-oxopurine base are good inhibitor

229 at the human acidic nuclear phosphoproteins (ANPs) ANP32A and ANP32B are functionally redundant but e

230 rocess called anaerobic, non-photosynthetic (ANP) mixotrophic fermentation.

231 eles are associated with higher human plasma ANP levels.

232 ooperative mechanism where Anxa6 potentiates ANP-dependent counterhypertrophic responses in cardiomyo

233 5I/Q568P had a reduced (38+/-7%, P<0.01) pro-ANP processing activity compared to that of wild type.

234 llular calcium (Ca(2+)) stimulated Anxa6-pro-ANP colocalization and membrane association.

235 utions occur, was required for efficient pro-ANP processing in functional assays.

236 ro-B-type NP), and MRproANP (midregional-pro-ANP) levels were 30%, 47%, and 18% lower in blacks compa

237 tes by facilitating regulated traffic of pro-ANP.

238 h decreased corin activity in processing pro-ANP.

239 ranules (SG) containing ANP propeptides (pro-ANP), a signature of maladaptive hypertrophy having coun

240 of neprilysin inhibition on mid-regional pro-ANP (MR-proANP), N-terminal pro-BNP (NT-proBNP), proBNP(

241 It also rescued pro-ANP translocation in cells expressing an Anxa6 mutant (A

242 We aimed to study the role of the pro-ANP convertase Corin in the pathogenesis of DN.

243 orin plays a renoprotective role through pro-ANP processing, and defects in Corin cause endothelial d

244 a6 mutants that failed to associate with pro-ANP hindered ANP-mediated protection against hypertrophy

245 pted a dynamic association of Anxa6 with pro-ANP-SG, parallel to their participation in anterograde t

246 Prolonged ANP exposure concomitantly reduced surface and total GC-

247 P production that could be targeted to raise ANP levels, which may have applications for the treatmen

248 ulator microRNA-425 (miR-425), which reduces ANP (atrial-NP) levels in whites.

249 microRNA 425 (miR-425) was found to regulate ANP production by binding to the mRNA of NPPA, the gene

250 a specific ANP receptor antagonist, reversed ANP's effect.

251 ry syndrome [ACS]) were genotyped for rs5065 ANP gene variant.

252 The MA of rs5065 ANP gene variant associates with increased susceptibilit

253 The size of SANPs, ANPs and GNPs was analyzed using a Coulter counter and t

254 le because these cells only express a single ANP receptor.

255 ough some aspects of heart maturation (size, ANP expression) are independent of GR at these key sites

256 Isatin, a specific ANP receptor antagonist, reversed ANP's effect.

257 In sum, ANP is an effective inhibitor of VEGF-induced vascular l

258 cal mapping studies in mice demonstrate that ANP sped electric conduction in the atria, whereas mANP

259 fluid balance, we tested the hypothesis that ANP or BNP (100 nM) would likewise elevate lymphatic per

260 We hypothesized that ANP would suppress near-term fetal cardiomyocyte prolife

261 eceptor in vitro Furthermore, we showed that ANP O-glycosylation attenuates acute renal and cardiovas

262 Taken together, our findings suggest that ANP-mediated cGMP signal transduction pathways regulate

263 A growing body of evidence suggests that ANP might be involved in the symptomology of alcohol dep

264 well as conditional triple mutants show that ANPs are required for elicitor-triggered defense respons

265 The ANP and B-type natriuretic peptide play an important rol

266 (5 muM) that was inhibited completely by the ANP receptor antagonist anantin and a 60% increase in ne

267 Recently, a mutation in the ANP gene, which results in the generation of a mutant fo

268 ed whether reactivity to alcohol cues in the ANP target region amygdala, a key area implicated in add

269 Moreover, the ANP-induced phosphorylation of VASP at Ser-239 is accomp

270 m the promoter region, and activation of the ANP gene.

271 NP73-102, the NH(2)-terminal peptide of the ANP prohormone, which down-regulates NPRA expression, al

272 use of a beta-cell-specific knockout of the ANP receptor with guanylate cyclase activity (betaGC-A-K

273 ally, suggesting polarized expression of the ANP receptors in these cells.

274 ANP can be measured by the magnitude of the ANP-induced increase in blood-to-tissue albumin transpor

275 Consistent with this, the ANP potently stimulated human trophoblasts in invading M

276 n a second phosphonate group attached to the ANP scaffold.

277 ting that Corin mediates its effects through ANP.

278 tidrug resistance (MDR) type 1, is linked to ANP expression on a bicistronic vector and was coexpress

279 Skin microcirculation responded to ANP similarly.

280 yed decreased cGMP production in response to ANP and BNP (all P<10(-6)), while cells expressing 541S

281 affect NPR-A function, the cGMP response to ANP and BNP was measured in cells expressing wild-type N

282 Our findings point to ANPs as key transduction elements that coordinate damage

283 rameshift product (fsANP), but not wild-type ANP (wtANP), was elevated in the serum of affected patie

284 tive was to compare the effects of wild-type ANP and mANP on atrial electrophysiology in mice and hum

285 fibrillation and demonstrate that wild-type ANP is antiarrhythmic.

286 zed MT and inactivation of Rho signaling via ANP-induced, PAK1-dependent inhibitory phosphorylation o

287 In vivo, ANP attenuated lung injury caused by excessive mechanica

288 In vivo, ANP significantly reduced VEGF-induced BRB leakage and t

289 lar Ca(2+) handling mechanisms through which ANP attenuates this sustained elevation in cytosolic Ca(

290 and 2.7 +/- 0.8-fold (P = 0.07, n = 7) with ANP and BNP, respectively.

291 that skeletal muscle albumin clearance with ANP treatment accounts for at most 30% of whole body cle

292 d, in skin and skeletal muscle compared with ANP alone (500 ng kg(-1) min(-1)).

293 eurohumoral properties of mANP compared with ANP were assessed in vivo in normal dogs.

294 wn structures of human HGPRT in complex with ANP-based inhibitors suggests reasons for the variations

295 tle with SIL+ISO yet rose nearly 5-fold with ANP, whereas protein kinase G activation (vasodilator-st

296 Similar effects were observed with ANP-siRNA transfection.

297 ed myoblasts only when applied together with ANP.

298 Confluent monolayers were treated with ANP or membrane-permeable cGMP analogs in the presence o

299 s in 62.5% of hearts, whereas treatment with ANP completely prevented the occurrence of arrhythmias.

300 in response to 100 nm Ang II with or without ANP (0.003-100 nm) or 1 microm 8-bromo-cGMP.